The most widely accepted model (Ross, et al, New England Journal of Medicine, 295, 369-377 and 420-425, 1976; and Friedman, et al, Prog. Hemostasis and Thrombosis, 4, 249-278, 1978) for the process of atherogenesis involves hemodynamic, immunologic or metabolic injury to the endothelial lining of a blood vessel, which causes the underlying smooth muscle layer to be exposed to blood elements. In this model, circulating platelets adhere to the damaged blood vessel wall, releasing their granule contents. This event appears to be vital in initiating the next step in the atherogenic process, which is the migration of smooth muscle cells from the medial layer of the blood vessel, where they normally reside, into the arterial intima (the inner layer of the vessel) and their subsequent proliferation. These intimal smooth muscle cells synthesize extracellular matrix material and imbibe lipid to produce the foam cells seen in atherosclerotic blood vessels. It is this overgrowth of smooth muscle cells, together with increased matrix material and lipid, which narrows the blood vessel lumen, compromising blood flow and causing an increased tendency for blood to clot and obstruct the affected vessel. Strategies for the prophylaxis and treatment of atherogenesis in the past have been directed at reducing risk factors for the disease, such as lowering blood pressure in hypertensive subjects, treating diabetics and reducing elevated cholesterol levels in hypercholesterolemic subjects.